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The swine-origin influenza A (H1N1) virus that burst into publicconsciousness a month ago is starting to behave like a mixture of itsinfamous, pandemic-causing predecessors.

It seems to have a predilection for young adults, as did its notoriousancestor, the 1918 Spanish influenza. Many of the young victims whohave become deathly ill turned out to have other medical problems -- aphenomenon first clearly seen with the1957 Asian flu. H 1N1 isspreading easily in North America but sputtering in Europe, just asHong Kong flu did in 1968. And as in the mini-pandemic of Russian fluin 1977, some people appear to have a degree of immunity.

Exactly how swine flu fits into the pantheon of flu pandemics will notbe known for a while. It will take months -- and many more victims --for its full personality and behavior to emerge. But one thing isclear: This is a lot more than just seasonal flu out of season.

After a brief moment when news of the outbreak in Mexico made swineflu look like a horseman of the apocalypse, public health officialshave spent much effort reassuring people that most of the time, thevirus causes a mild illness that can be ridden out at home. Yet,officials at the World Health Organization, the Centers for DiseaseControl and Prevention and elsewhere do not want the public to getblase.ad_icon

Pandemic flu strains -- and this new H1N1 strain is all but certain tocause the 21st century's first pandemic -- are unpredictable. Anycontagious disease that most of the world's 6.8 billion people cancatch is inherently dangerous.

"Our message to everybody is, of course, do not over-worry about thesethings, [but] it is important to know it is serious," the WHO's KeijiFukuda said last week.

Perhaps the most worrisome features so far are the number and severityof cases in teenagers and young adults. This was noticed early, andthe pattern has not changed much now that there are 5,000 laboratory-confirmed infections and probably more than 100,000 overall. Theaverage age of the confirmed and probable cases is 15 years. Two-thirds are younger than 18.

There are two theories for what is happening.

One is that students visiting Mexico on spring break were the chief"vectors" bringing the virus to the United States, where they theninfected schoolmates and friends. The other is that young people areespecially vulnerable for some reason.

"As we get farther and farther in, are we going to be able to choosebetween these two hypotheses? Sure we are," Joseph Bresee, the CDC'schief flu epidemiologist, said late last week. But, he added, it maytake two or three months.

Determining the true age distribution is crucial, as it will help setthe policy for who should be first in line for vaccines and how toration antiviral drugs if they are in short supply. "It really doeshave big implications," Bresee said.

A closely related question is whether the illness tends to be moreserious in younger age groups as well as more common.

In the United States, the familiar seasonal influenza causes about8,100 deaths a year directly and contributes to about 36,000 more inpeople with lung or heart problems. Ninety percent of those deathsoccur in people 65 and older. The risk of a healthy person older than65 dying directly from flu is about 100 times that of a healthy person5 to 49 years old.

Compared with seasonal outbreaks, all flu pandemics cause a higherpercentage of severe cases and deaths in younger groups. Although theoverall mortality rate from the current swine flu is low, this trendis already apparent.

Last Thursday, when Fukuda announced that the global death total was65, he noted that "half of them are healthy people who have nopredisposing conditions. This is a pattern different from what we seewith normal influenza."

There have been too few deaths in the United States to draw anyconclusions. But of the 173 people who have been sick enough to behospitalized, more than half are in the 5-to-24 age group.

In the 1918 pandemic, which killed at least 50 million people, nearlyhalf the deaths were of people 20 to 40 years old. More than 95percent were of people younger than 65. In comparison, 36 percent ofthe deaths in the 1957 pandemic were of people younger than 65, and 48percent in the 1968 pandemic.

The 1918 pattern has led many experts to speculate that older peoplemay have had immunity from a "Spanish-like" virus that circulated intheir youth, sometime before about 1885. Something similar may behappening this time.

The H1 and N1 in the name of the new strain refer to proteins on thevirus's surface. The human immune system "sees" them and tailor-makesantibodies to attack the bug. Flu vaccines work by priming the immunesystem with harmless versions of the same H and N proteins.

A variety of H1N1 strains circulated from 1918 to 1957, thendisappeared for two decades. In 1977, however, an H1N1 strain surfacedthat was nearly identical to the previous one, so much so thatscientists suspect it was an accidental release from a lab freezer. Itcaused a pandemic -- Russian flu -- that was largely limited to peopleyounger than 25, whose immune systems had never experienced H1N1.

Strains of H1N1 have continuously circulated since then. While the newone is very different -- the H and N proteins are from pig, not human,viruses -- decades of exposure to H1N1s may be providing older peoplewith some protection. Some young people may have had essentially noexposure.

"My first speculation is that this younger population has somehowmissed contact with H1N1 or with vaccine," said Edwin D. Kilbourne, anemeritus professor at New York Medical College and, at 88, fluvirology's elder statesman in the United States.

Differences in background immunity may also exist across geographicalareas. This is the reason for the big difference in North America'sand Europe's experience with the 1968 Hong Kong flu, a pandemic thatspanned two winters.

In the United States, nearly three-quarters of all deaths that wereultimately attributed to that flu came in the first winter(1968-1969). In England and France, more than three-quarters were inthe second winter (1969-1970).

In that virus, one old surface protein, the H, was switched out for anew one in a process called reassortment. The strain went from H2N2 toH3N2. Epidemiologists now believe that Europeans had had more recentand intense exposure to H2N2 viruses than North Americans.Consequently, Europeans had developed antibodies and were partiallyprotected when the "half-new" H3N2 strain arrived.

By the second winter, however, the N2 part of the virus had alsochanged somewhat through mutations and was no longer very recognizableto the immune system. The antibodies that had protected a lot ofEuropeans the previous winter no longer worked against this "drifted"strain of H3N2. Cases of flu -- and deaths -- went way up.

Whether a similar difference in continent-wide susceptibility explainswhy swine flu is spreading in the United States but standing still inEurope will take a while to figure out.